Aging is associated with a reduction in metabolic insulin action, which may increase the susceptibility of older people to develop diabetes mellitus. Although the development of insulin resistance has been attributed to a decrease insulin action in aged skeletal muscle, aging per se is probably not the cause of insulin resistance. Both a decrease in physical activity and an increase in body fat and corresponding decrease in LBM may be responsible for the development of insulin resistance. A number of studies have examined the effect of aerobic exercise training to improve insulin sensitivity in older adults. To date, no studies have examined the effect of strength training on insulin-mediated vasodilatation nor endothelium-derived nitric oxide production and its role in increasing metabolic insulin action. To examine the effect of strength training on these parameters non-smoking, non-diabetic men and women age 50-70 yrs will undergo a 16 week program of upper and lower body strength training alone or combined. At baseline and after 16 weeks of strength training the subjects will have insulin sensitivity determined by a hyperinsulinemic euglycemic clamp, with simultaneous measurement of arm and leg basal and insulin-mediated blood flow, as well as measurement of nitric oxide biomarkers in the leg and arm. Lean body mass (LBM) will be determined by dual energy photon absorptiometry (DEXA), and blood pressure (BP) responses determined by 24 hr ambulatory BP. To determine the effect of increased muscle mass and the local effects of strength training on insulin-mediated vasodilatation, subjects will undergo one of three regular strength training programs. One group will undergo upper body only strength training, a second group will undergo lower body strength training and a third group will undergo a combined program of both upper and lower body strength training. Subjects will be assigned to one of the three groups by picking numbers out of a hat. We expect that the improvements in metabolic insulin action will be due in part to an increase in both insulin-mediated blood flow and endothelium-derived nitric oxide production. However, the enhancements in insulin-mediated blood and endothelium-derived nitric oxide production will be localized to only the exercising muscles. The design of this study will allow us to gain insight into the mechanism by which metabolic insulin is improved.